Shock is a condition in which lack of substrate and oxygen transport to the cell results in a great insult to the mitochondrion. Detection of altered mitochondrial function in shock at an early and potentially reversible stage is critical. At present no completely satisfactory method is available to assess the adequacy of oxygen availability to a vital organ. Currently available parameters, such as arterial or venous oxygen tensions, are indirect and uncertain since the critical function to be maintained is assumed to be aerobic mitochondrial metabolism. The use of differential spectrophotometry provides a means of monitoring the redox state of mitochondrial cytochromes in vivo in exposed cerebral cortex as a parameter relevant to the state of mitochondrial activity. The incident monochromatic light is absorbed in transit by specific cytochrome depending upon the wavelength selected. Since cytochromes absorb light differently in oxidized and reduced state, the redox state of these carriers can be analyzed spectrophotometrically without inducing changes n aerobic metabolic function. Using this technique, we have previously demonstrated, in vivo, shifts in the redox state of cytochrome a,a3 toward reduction in hemorrhagic shock in cats. This technique has recently been used noninvasively (close skull). It is the purpose of this research proposal to: 1) extend the previous observations in order to detect the mitochondrial insult resulting from shock at an early stage before it becomes irreversible, 2) evaluate the effects of reinfusion of shed blood and glucocorticoids, as well as hyperbaric oxygenation on the redox state of cytochrome a,a3 following the induction of shock and 3) accomplish a totally noninvasive in vivo spectrophotometric study of the mitochondrial oxygenation state for constant monitoring of the pathophysiological consequences of shock. If successful, the latter technique can be applied readily to man.